This study will evaluate the relationship(s) between hemodynamics, plasma volume, and exchangeable sodium in the etiology of increased total peripheral resistance seen with salt-induced hypertension in rats. Specifically, it will establish: 1) Whether or not an autoregulatory mechanism is involved in the development of salt-induced hypertension in genetically predisposed rats (Dahl strains), versus rats with renal impairment (subtotal nephrectomy), versus rats with mineralocorticoid-type hypertension (DOCA). There is presumptive evidence from the literature that a common autoregulatory mechanism may be involved, at least in part, in these three models of salt-induced hypertension. 2) Are there changes in autoregulatory responsiveness related to the duration of hypertension? Of particular interest will be strain-dependent differences in autoregulatory responsiveness (i.e., Dahl salt-resistant (R) versus salt-sensitive (S) rats. These studies will be performed in conscious rats instrumented with electromagnetic flow probes and arterial catheters. Data collection will be performed continuously by computer for increased accuracy and reduced animal/experimenter interaction. Previous studies have not systematically analyzed hemodynamic changes (as a function of time and in the conscious animal) associated with the development of salt-induced hypertension in the rat. In addition, no single study has compared the hemodynamics of these three models under the same experimental protocols. The results of the proposed study should help distinguish between hemodynamic and non-hemodynamic mechanisms involved in the genesis of an elevated total peripheral resistance in salt-induced hypertension. This should provide some insight into the pathophysiological changes associated with hypertension related to increased levels of salt intake.